Epilepsy is a neurological disorder manifested by rapid and recurrent seizures, resulting from synchronized discharges of neurons in brain, affecting at least 1% of the world population To explain the mechanism how seizures are generated in specific brain areas or different brain structures, various studies have been performed worldwide involving behavioral, electrophysiological and molecular analysis. So far, the immense majority of epilepsy research has been executed in rodents and stimulation of neurons by electrical or chemical induction resulting in seizure discharges is believed to be the most common way to contribute to the process of epileptogenesis referred as “kindling.”
In kindling, an initially sub-convulsive chemical or electrical convulsant stimulus of the brain evokes seizure discharges. The molecular mechanisms underlying the development of the abnormal excitability in kindling or epilepsy are poorly understood. However, it is believed that structural rearrangements responsible for maintenance of epileptic syndrome might be triggered by trophic factors such as BDNF (brain derived neurotrophic factor) that is involved in various signaling mechanisms that may be influenced by seizure activity. Among various trophic factors, much interest has been focused on the BDNF, NGF, and NT-3, and their high-affinity receptors TrkA, TrkB and TrkC. Variety of epilepsy models have shown that seizure activity induces transient changes of neurotrophin gene expression in neurons. In addition to these trophic factors, the proto-oncogene c-fos has also been shown to be induced transiently in response to various stimuli such as seizures induction. The c-fos gene encodes a DNA-binding protein, c-Fos, which forms a heterodimeric transcriptional factor, activator protein-1 (AP-1) by direct participation or with c-jun. The activation of c-fos expression in neurons by seizures led to its proposed use as a marker of neuronal activity.